PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29229994-2 2018 By directly activating Bax/Bak with BH3-only proteins or BH3 mimetic compounds, we demonstrate that mitochondrial damage correlated with a rapid increase in intracellular [AMP]/[ATP], phosphorylation of 5" AMP-activated protein kinase (AMPK), and activation of unc-51 like autophagy activating kinase 1 (ULK1). Adenosine Triphosphate 178-181 BCL2 associated X, apoptosis regulator Homo sapiens 23-26 26491047-0 2016 ATP promotes cell survival via regulation of cytosolic [Ca2+] and Bcl-2/Bax ratio in lung cancer cells. Adenosine Triphosphate 0-3 BCL2 associated X, apoptosis regulator Homo sapiens 72-75 26816615-8 2016 The results showed that knockdown of CLIC4 with or without 100 muM adenosine triphosphate (ATP) treatment significantly increased the expression of Bax, active caspase 3, active caspase 4 and CHOP but suppressed Bcl-2 expression in HN4 cells. Adenosine Triphosphate 67-89 BCL2 associated X, apoptosis regulator Homo sapiens 148-151 26816615-8 2016 The results showed that knockdown of CLIC4 with or without 100 muM adenosine triphosphate (ATP) treatment significantly increased the expression of Bax, active caspase 3, active caspase 4 and CHOP but suppressed Bcl-2 expression in HN4 cells. Adenosine Triphosphate 91-94 BCL2 associated X, apoptosis regulator Homo sapiens 148-151 26491047-3 2016 We examined ATP-induced Ca(2+) signaling and its effects on antiapoptotic (Bcl-2) and proapoptotic (Bax) proteins in normal human airway epithelial cells and lung cancer cells. Adenosine Triphosphate 12-15 BCL2 associated X, apoptosis regulator Homo sapiens 100-103 26491047-8 2016 The Bcl-2/Bax ratio was increased in lung cancer cells following treatment with ATP; however, the antiapoptotic protein Bcl-2 demonstrated more sensitivity to ATP than proapoptotic protein Bax. Adenosine Triphosphate 80-83 BCL2 associated X, apoptosis regulator Homo sapiens 10-13 24308865-6 2014 We concluded that the increase in cytosolic cytochrome c and available intracellular ATP should be responsible for the increase in caspase-9 activity; the activation of caspase-9 could be limited by the subsequent depletion of ATP; the postmortem release level of cytochrome c could be determined by the ratio of bax to bcl-2 in fresh tissues. Adenosine Triphosphate 85-88 BCL2 associated X, apoptosis regulator Homo sapiens 313-316 26491047-8 2016 The Bcl-2/Bax ratio was increased in lung cancer cells following treatment with ATP; however, the antiapoptotic protein Bcl-2 demonstrated more sensitivity to ATP than proapoptotic protein Bax. Adenosine Triphosphate 159-162 BCL2 associated X, apoptosis regulator Homo sapiens 10-13 26491047-9 2016 Decreasing extracellular Ca(2+) or chelating intracellular Ca(2+) with BAPTA-AM significantly inhibited ATP-induced increase in Bcl-2/Bax ratio, indicating that a rise in [Ca(2+)]cyt through Ca(2+) influx is the critical mediator for ATP-mediated increase in Bcl-2/Bax ratio. Adenosine Triphosphate 104-107 BCL2 associated X, apoptosis regulator Homo sapiens 134-137 26491047-9 2016 Decreasing extracellular Ca(2+) or chelating intracellular Ca(2+) with BAPTA-AM significantly inhibited ATP-induced increase in Bcl-2/Bax ratio, indicating that a rise in [Ca(2+)]cyt through Ca(2+) influx is the critical mediator for ATP-mediated increase in Bcl-2/Bax ratio. Adenosine Triphosphate 104-107 BCL2 associated X, apoptosis regulator Homo sapiens 265-268 26491047-11 2016 Increasing the Bcl-2/Bax ratio by exposure to high extracellular ATP may, therefore, be an important selective pressure promoting transformation and cancer progression. Adenosine Triphosphate 65-68 BCL2 associated X, apoptosis regulator Homo sapiens 21-24 24961145-11 2014 We further investigated the potential mechanisms involved in the inhibitory effect of extracellular ATP on the growth of NPC cells and found that extracellular ATP could reduce Bcl-2 and p-AKT levels while elevating Bax and cleaved caspase-3 levels in NPC cells. Adenosine Triphosphate 160-163 BCL2 associated X, apoptosis regulator Homo sapiens 216-219 18691757-3 2009 375 distinct proteins were identified where ATP-dependent RNA helicase DDX3, HNRPU, Matrin-3, Importin-7 and Bax were among the 25 most upregulated proteins and Hausp/UBP7, UBE2N and ERp29 among the 17 most downregulated. Adenosine Triphosphate 44-47 BCL2 associated X, apoptosis regulator Homo sapiens 109-112 21430642-3 2011 We exposed renal epithelial cells to metabolic stress causing ATP depletion in the absence of glucose and found that this activated glycogen synthase kinase 3beta (GSK3beta) and Bax caused mitochondrial membrane injury and apoptosis. Adenosine Triphosphate 62-65 BCL2 associated X, apoptosis regulator Homo sapiens 178-181 21289292-4 2011 Oxygen consumption and cellular ATP levels were reduced in BAX-deficient cells, while glycolysis was increased. Adenosine Triphosphate 32-35 BCL2 associated X, apoptosis regulator Homo sapiens 59-62 21289292-5 2011 These results suggested that cells lacking BAX have a deficiency in the ability to generate ATP through cellular respiration. Adenosine Triphosphate 92-95 BCL2 associated X, apoptosis regulator Homo sapiens 43-46 21289292-8 2011 Inhibition of BAX with small interfering RNAs reduced intracellular ATP content in BAX-containing cells. Adenosine Triphosphate 68-71 BCL2 associated X, apoptosis regulator Homo sapiens 14-17 21289292-8 2011 Inhibition of BAX with small interfering RNAs reduced intracellular ATP content in BAX-containing cells. Adenosine Triphosphate 68-71 BCL2 associated X, apoptosis regulator Homo sapiens 83-86 21289292-9 2011 Expression of either full-length or COOH-terminal-truncated BAX in BAX-deficient cells rescued ATP synthesis and oxygen consumption and reduced glycolytic activity, suggesting that this metabolic function of BAX was not dependent upon its COOH-terminal helix. Adenosine Triphosphate 95-98 BCL2 associated X, apoptosis regulator Homo sapiens 60-63 21289292-10 2011 Expression of BCL-2 in BAX-containing cells resulted in a subsequent loss of ATP measured, implying that, even under nonapoptotic conditions, an antagonistic interaction exists between the two proteins. Adenosine Triphosphate 77-80 BCL2 associated X, apoptosis regulator Homo sapiens 23-26 18160625-11 2008 Consistently, wild-type and mitochondrial Bcl-2, but not ER-Bcl-2, blocked Bax activation during ATP depletion, a critical event for mitochondrial outer membrane permeabilization and cytochrome c release. Adenosine Triphosphate 97-100 BCL2 associated X, apoptosis regulator Homo sapiens 75-78 18546202-7 2008 The data demonstrate that apoptosis in HeLa cells is ATP dependent and requires the translocation of Bax. Adenosine Triphosphate 53-56 BCL2 associated X, apoptosis regulator Homo sapiens 101-104 18357533-6 2008 At the 4/2 time point, FeTMPyP also partially inhibited the ATP depletion mediated increase in tumor necrosis factor alpha (TNF-alpha) and decreased Bax and FasL gene expression. Adenosine Triphosphate 60-63 BCL2 associated X, apoptosis regulator Homo sapiens 149-152 18771651-6 2008 ATP or a combination of cyclosporin A and ADP, inhibitors of the mPT, suppressed BAX(oligo)-induced mitochondrial swelling and depolarization as well as cytochrome c release but did not influence BAX(oligo) insertion into the OMM. Adenosine Triphosphate 0-3 BCL2 associated X, apoptosis regulator Homo sapiens 81-84 18753054-0 2008 [Bax is involved in K ATP-mediated protection of the hippocampal neurons against hypoxic exposure]. Adenosine Triphosphate 22-25 BCL2 associated X, apoptosis regulator Homo sapiens 1-4 15578915-7 2004 The release of cytochrome c from mitochondria to the cytosol during apoptosis is mediated by the mitochondrial permeability transition pore, which is a protein complex formed by the voltage-dependent anion channel, members of the pro- and anti- apoptotic Bax-Bcl-2 protein family, cyclophilin D, and adenine nucleotide (ADP/ATP) translocators. Adenosine Triphosphate 324-327 BCL2 associated X, apoptosis regulator Homo sapiens 255-258 17692540-4 2007 The ability of TCR-dependent Ca(2+) signals to stimulate mitochondrial NADH production in excess of that utilized for ATP synthesis was dependent on Bax and Bak. Adenosine Triphosphate 118-121 BCL2 associated X, apoptosis regulator Homo sapiens 149-152 15784164-7 2005 The changes in HSP60, Bax and cytochrome c during hypoxia can be replicated by ATP depletion. Adenosine Triphosphate 79-82 BCL2 associated X, apoptosis regulator Homo sapiens 22-25 15755925-2 2005 In in vitro models, ATP depletion-induced apoptosis of tubular cells is mediated by the intrinsic pathway involving Bax translocation, cytochrome c release, and caspase activation. Adenosine Triphosphate 20-23 BCL2 associated X, apoptosis regulator Homo sapiens 116-119 15752543-5 2005 This result suggests the presence of a certain mechanism independent of Bax inactivation to increase ATP levels of cells under non-apoptotic condition. Adenosine Triphosphate 101-104 BCL2 associated X, apoptosis regulator Homo sapiens 72-75 10725400-6 2000 We also established a cell-free Bax degradation assay in which an in vitro-translated, (35)S-labeled Bax protein can be degraded by a tumor cell protein extract, inhibitable by addition of a proteasome inhibitor or depletion of the proteasome or ATP. Adenosine Triphosphate 246-249 BCL2 associated X, apoptosis regulator Homo sapiens 32-35 15113746-9 2004 In ATP-depleted cells, Zn(2+) partially prevented Bax activation and cytochrome c release from mitochondria. Adenosine Triphosphate 3-6 BCL2 associated X, apoptosis regulator Homo sapiens 50-53 12543814-3 2003 Conversely, Bax, which displaces Bcl-2 from ANT in apoptotic cells, inhibits ADP/ATP exchange through a direct action on ANT. Adenosine Triphosphate 81-84 BCL2 associated X, apoptosis regulator Homo sapiens 12-15 12543814-4 2003 The Bax-mediated inhibition of ADP/ATP exchange can be separated from Bax-stimulated formation of nonspecific pores by ANT. Adenosine Triphosphate 35-38 BCL2 associated X, apoptosis regulator Homo sapiens 4-7 15481605-5 2004 The Bcl-2/ Bax mRNA expression ratio increased progressively from the control to the heat preconditioned and ATP depleted cells (control; 100%, ATP depletion; 154 +/- 6%, heat preconditioning; 212 +/- 6%, heat preconditioning and ATP depletion; 421 +/- 8%). Adenosine Triphosphate 109-112 BCL2 associated X, apoptosis regulator Homo sapiens 11-14 15481605-5 2004 The Bcl-2/ Bax mRNA expression ratio increased progressively from the control to the heat preconditioned and ATP depleted cells (control; 100%, ATP depletion; 154 +/- 6%, heat preconditioning; 212 +/- 6%, heat preconditioning and ATP depletion; 421 +/- 8%). Adenosine Triphosphate 144-147 BCL2 associated X, apoptosis regulator Homo sapiens 11-14 15481605-5 2004 The Bcl-2/ Bax mRNA expression ratio increased progressively from the control to the heat preconditioned and ATP depleted cells (control; 100%, ATP depletion; 154 +/- 6%, heat preconditioning; 212 +/- 6%, heat preconditioning and ATP depletion; 421 +/- 8%). Adenosine Triphosphate 144-147 BCL2 associated X, apoptosis regulator Homo sapiens 11-14 15481605-8 2004 CONCLUSION: There may be a possibility that the preservation of cytolytic damage and an increase in the Bcl-2/Bax mRNA expression ratio is related to the increase of HSP72 in ATP depletion as a hypoxia model. Adenosine Triphosphate 175-178 BCL2 associated X, apoptosis regulator Homo sapiens 110-113 15183659-5 2004 The expression of the proapototic protein Bax increased as an inverse function with cerebral tissue ATP and phosphocreatine concentrations. Adenosine Triphosphate 100-103 BCL2 associated X, apoptosis regulator Homo sapiens 42-45 12915121-3 2003 In apoptosis triggered by ATP depletion, the proapoptotic molecule Bax translocated from the cytosol to mitochondria, followed by cytochrome c release from the organelle, caspase activation, and development of apoptotic morphology. Adenosine Triphosphate 26-29 BCL2 associated X, apoptosis regulator Homo sapiens 67-70 12606781-0 2003 Poly(ADP-ribose) polymerase activation and changes in Bax protein expression associated with extracellular ATP-mediated apoptosis in human embryonic kidney 293-P2X7 cells. Adenosine Triphosphate 107-110 BCL2 associated X, apoptosis regulator Homo sapiens 54-57 12606781-6 2003 An ATP-induced decrease in the pro-apoptotic bax gene expression was detected by apoptosis-related cDNA microarray analysis, which correlated with a decrease of Bax protein expression. Adenosine Triphosphate 3-6 BCL2 associated X, apoptosis regulator Homo sapiens 45-48 12606781-6 2003 An ATP-induced decrease in the pro-apoptotic bax gene expression was detected by apoptosis-related cDNA microarray analysis, which correlated with a decrease of Bax protein expression. Adenosine Triphosphate 3-6 BCL2 associated X, apoptosis regulator Homo sapiens 161-164 12606781-8 2003 Both ATP-induced molecular alterations in HEK-P2X(7) cells (i.e., decrease of Bax expression and increase of PARP cleavage) were blocked by the purinergic P2X(7) receptor antagonist oxidized ATP. Adenosine Triphosphate 5-8 BCL2 associated X, apoptosis regulator Homo sapiens 78-81 12606781-8 2003 Both ATP-induced molecular alterations in HEK-P2X(7) cells (i.e., decrease of Bax expression and increase of PARP cleavage) were blocked by the purinergic P2X(7) receptor antagonist oxidized ATP. Adenosine Triphosphate 191-194 BCL2 associated X, apoptosis regulator Homo sapiens 78-81 12022947-3 2002 Among the various PTPC components, the adenine nucleotide translocator (ANT) appears to act as a bi-functional protein which, on the one hand, contributes to a crucial step of aerobic energy metabolism, the ADP/ATP translocation, and on the other hand, can be converted into a pro-apoptotic pore under the control of onco- and anti-oncoproteins from the Bax/Bcl-2 family. Adenosine Triphosphate 211-214 BCL2 associated X, apoptosis regulator Homo sapiens 354-357 11526446-5 2001 The mitochondria uncoupler FCCP, in the presence of the F(1)-F(0) ATPase inhibitor oligomycin, can trigger Bax translocation to mitochondria suggesting that when ATP levels are maintained a collapse of DeltaPsi(m) induces Bax translocation. Adenosine Triphosphate 66-69 BCL2 associated X, apoptosis regulator Homo sapiens 107-110 11526446-7 2001 Bax association with mitochondria is also triggered by inhibitors of the electron transport chain, antimycin and rotenone, compounds that collapse DeltaPsi(m) without inducing rapid ATP hydrolysis that typically occurs with uncouplers such as FCCP. Adenosine Triphosphate 182-185 BCL2 associated X, apoptosis regulator Homo sapiens 0-3 11279112-1 2001 ATP depletion results in Bax translocation from cytosol to mitochondria and release of cytochrome c from mitochondria into cytosol in cultured kidney cells. Adenosine Triphosphate 0-3 BCL2 associated X, apoptosis regulator Homo sapiens 25-28 11279112-4 2001 Now we show that translocated Bax forms homo-oligomeric structures, stabilized as chemical adducts by bifunctional cross-linkers in ATP-depleted wild type cells, but remains monomeric in Bcl-2-overexpressing cells. Adenosine Triphosphate 132-135 BCL2 associated X, apoptosis regulator Homo sapiens 30-33 10725400-6 2000 We also established a cell-free Bax degradation assay in which an in vitro-translated, (35)S-labeled Bax protein can be degraded by a tumor cell protein extract, inhibitable by addition of a proteasome inhibitor or depletion of the proteasome or ATP. Adenosine Triphosphate 246-249 BCL2 associated X, apoptosis regulator Homo sapiens 101-104 10030664-2 1998 During glucose-free hypoxia, cell ATP levels declined steeply resulting in the translocation of Bax from cytosol to mitochondria. Adenosine Triphosphate 34-37 BCL2 associated X, apoptosis regulator Homo sapiens 96-99 10656679-6 2000 Cooperative channel formation by Bax and ANT is stimulated by the ANT ligand atractyloside (Atr) but inhibited by ATP, indicating that it depends on the conformation of ANT. Adenosine Triphosphate 114-117 BCL2 associated X, apoptosis regulator Homo sapiens 33-36